Jaffe A, Vinella D, D'Ari R
Institut Jacques Monod (Centre National de la Recherche Scientifique, Universite Paris 7), France.
J Bacteriol. 1997 Jun;179(11):3494-9. doi: 10.1128/jb.179.11.3494-3499.1997.
Escherichia coli hupA hupB double mutants, lacking both subunits (HU1 and HU2) of the histone-like protein HU, accumulate secondary mutations. In some genetic backgrounds, these include mutations in the minCDE operon, inactivating this system of septation control and resulting in the formation of minicells. In the course of the characterization of hupA hupB mutants, we observed that the simultaneous absence of the HU2 subunit and the MukB protein, implicated in chromosome partitioning, is lethal for the bacteria; the integrity of either HU or MukB thus seems to be essential for bacterial growth. The HU protein has been shown to be involved in DNA replication in vitro; we show here that its inactivation in the hupA hupB double mutant disturbs the synchrony of replication initiation in vivo, as evaluated by flow cytometry. Our results suggest that global nucleoid structure, determined in part by the histone-like protein HU, plays a role in DNA replication initiation, in proper chromosome partitioning directed by the MukFEB proteins, and in correct septum placement directed by the MinCDE proteins.
大肠杆菌hupA hupB双突变体缺乏类组蛋白HU的两个亚基(HU1和HU2),会积累二次突变。在某些遗传背景下,这些突变包括minCDE操纵子中的突变,使这种细胞分裂控制系统失活,导致微细胞形成。在对hupA hupB突变体的表征过程中,我们观察到,同时缺失HU2亚基和参与染色体分配的MukB蛋白对细菌是致死的;因此,HU或MukB的完整性似乎对细菌生长至关重要。已证明HU蛋白在体外参与DNA复制;我们在此表明,通过流式细胞术评估,其在hupA hupB双突变体中的失活会干扰体内复制起始的同步性。我们的结果表明,部分由类组蛋白HU决定的整体核仁结构在DNA复制起始、由MukFEB蛋白指导的正确染色体分配以及由MinCDE蛋白指导的正确隔膜定位中发挥作用。